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1 se-activated receptor-specific manner during nephrosis.
2 ular damage and podocyte loss induced by PAN nephrosis.
3 ith histopathological findings of congenital nephrosis.
4 response to puromycin aminonucleoside (PAN) nephrosis.
5 function in a rat model of puromycin-induced nephrosis.
6 ween these processes in rats with adriamycin nephrosis.
7 ause of loss of renal function in adriamycin nephrosis.
8 induction of puromycin aminonucleoside (PAN) nephrosis.
9 lointerstitial nephritis associated with PAN nephrosis.
10 uria and how it causes the other findings of nephrosis.
11 pment, abnormal extrapyramidal movements and nephrosis.
12 that transcript levels of the podocyte gene nephrosis 2 homolog (Nphs2), were heritable and controll
13 5.15) for nephritis, nephrotic syndrome, and nephrosis; 4.08 (1.38-12.08) for esophageal cancer; 4.19
14 dence of proteinuria, indicated by relapsing nephrosis after CsA withdrawal, required additional cour
15 Most aging rats display chronic progressive nephrosis, although the rate at which injury develops is
18 in 1 (RIP1) kinase domain, prevented osmotic nephrosis and CIAKI, whereas an inactive Nec-1 derivate
19 linical CIAKI, including RCM-induced osmotic nephrosis and increased serum levels of urea and creatin
20 In the human glomerulopathies minimal-change nephrosis and membranous nephropathy, there is an increa
21 Developments related to the pathogenesis of nephrosis and why some patients develop focal segmental
22 a as a contributor to podocyte injury during nephrosis, and suggest that thrombin and/or podocyte-exp
24 ncer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory disease, and influe
25 he podocytes, leading to the hypothesis that nephrosis develops from an inability to develop a functi
28 t the induction of puromycin aminonucleoside nephrosis involves podocyte migration conducted by a coo
30 d glomerulopathies, including minimal change nephrosis, membranous glomerulonephritis, and IgA nephro
31 he nephrotic syndrome, the murine adriamycin nephrosis model was used to explore the role of RAGE in
32 rthermore, the rat puromycin aminonucleoside nephrosis model, previously suspected of undergoing SD-T
34 with hirudin reduced proteinuria in two rat nephrosis models, and thrombin colocalized with a podocy
38 d disorder characterized by microcephaly and nephrosis resulting from mutations in the WDR73 gene.
39 y, serologic, and histopathologic indices of nephrosis showed reversal of CG in 8 of 12 CYC202-treate
40 lasma thrombin generation is enhanced during nephrosis, suggesting that thrombin may contribute to ne
43 Wistar albino rat shows progressive chronic nephrosis with age and therefore was used to determine t
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